Methylation reactions increase in aging, the symptoms of Parkinson’s Disease (PD) are strikingly similar to the neurological and functional changes seen in advanced aging, and Parksinson’s Disease is age-related. For methylation to be regarded as important in PD it means that, along with its biochemical reactions and behavioral effects, increased methylation should also cause specific neuronal degeneration . . . Most of the SAM-induced anatomical changes that were observed in the rat model are similar to the changes that occur in PD, which further support a role of SAM-dependent increased methylation in PD.[1]

and . . .

Increased methylation can deplete dopamine, norepinephrine and 5-HT; increase acetylcholine; and cause hypokinesia and tremors. These effects are similar to changes seen in PD, and interestingly also, they are similar to some of the changes that are associated with the aging process. It is suggested, therefore, that increased methylation may be an inducing factor in parkinsonism. Accordingly, the effects of an increase in methylation in the brain of rats were studied. S-adenosylmethionine (AdoMet), the limiting factor in the methylation process, was injected into the lateral ventricle of rats. Specific behavioral changes that resemble changes seen in PD were investigated. The results showed that AdoMet caused tremors, rigidity, hypokinesia, and depleted DA.[2]

Possible, if you supplement with high dose of methylfolate. Another option would be to use calcium folinate or a combination of both instead. Nicotinic acid (niacin) supposedly acts as a methyl sponge and might be able to counteract excess methyl groups. Also, according to some sources the gut plays a major role in aggravating certain pathways and can lead to overmethylation. Unfortunately, it is very individual and depends on so many variables...